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Through a study of human genetics in different populations around the world, researchers at the Pasteur Institute and CNRS have discovered how pathogens may vary over time the evolution of our immune system. It is as if, unlike viruses, bacteria, fungi and parasites seem to have allowed the introduction of mutations in the genes of certain immune system proteins, thus allowing greater genetic variability. In some cases, these mutations may even be an advantage, giving the host a better human resistance to infectious diseases such as leprosy or tuberculosis.

Researchers at the Institut Pasteur and CNRS, in the unity of human evolutionary genetics, just published in the journal PLoS Genetics is the study showing the influence of relationships between humans and pathogens . Scientists have studied why the genetic variability of ten proteins of the innate immune system, the first line of defense against these agents which attack our body. These proteins are a family of receptors called TLR (for Toll-like receptors) and are responsible for recognizing pathogens to trigger an immune response and eliminate them. 

The researchers showed a strong similarity in different populations around the world are recognizing genes TRL viruses: mutations are very rare, and the level of sequence conservation of these genes is extreme. Viruses have exerted over time a very strong selective pressure on these proteins, preventing them from genetic evolution. In contrast, the genes for TLRs recognize bacteria, fungi or parasites show a greater variability: it seems possible that mutations accumulate without any concern for the organization. This suggests that the role of these proteins is not essential. 

This research corroborated the observations showing that the few known mutations affecting the genes of receptors TLR "virus" are the source of rare and serious diseases. This is the case for a mutation that affects the gene TLR 3, which was previously identified as responsible for encephalitis. The mutations affecting the genes of other types of TRL, they cause or contribute to infectious disease less severe and more frequent. One of the mutations affecting TLR 6 gene is for example to a predisposition to asthma in children. 

Through this study, scientists were also able to show that a mutation affecting the receptor TLR1, designed to identify bacteria, could be an advantage! Found in two out of five in Europe, this mutation has the effect of preventing the expression of this receptor on the surface of cells and therefore reduce from 40 to 60% in the inflammatory response. In previous studies, this mutation has been associated with greater resistance vis-à-vis leprosy and tuberculosis. 

The evolutionary approach to the study sheds light on the original issue of relations between men and pathogens. From the direct analysis of genetic sequences, it opens up avenues to explore from a clinical, immunological and epidemiological research to better understand the susceptibility to certain diseases. 

Tags:	pathogens - immune system. - human resistance - TLRs - CNRSrecognize bacteria -
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